Chlorinated pesticides such as DDT, chlordecone, lindane, methoxychlor, toxaphene and dieldrin are recognized for their neuroexcitatory effects. Many are also recognized for their reproductive toxicity but, until recently, few attempts had been made to relate these two manifestations. After a relatively short-term exposure condition in female rats chlordecone has been demonstrated to alter several indices of females reproductive competence including inhibition of estrogen mediated changes in CNS progesterone receptors, pituitary LH release and sexual behavior. Chlordecone disrupted estrous cycle changes in serotonin receptors and reduced fertility under various exposure conditions. Results of these studies have suggested a dual mode of neuro- reproductive toxicity exerted by chlorinated pesticides. One mode involves the pesticide's antiestrogenic action at the CNS estrogen receptor and the other involves the disruption of neurotransmitter function. Disruptions of reproductive behaviors after diestrous exposure rely primarily upon antiestrogenic actions while exposure near the period of ovulation may involve serotonergic mechanisms. The proposed studies are designed to evaluate this dual mechanism hypothesis. These studies are of considerable health significance since it has been thought that the "estrogenicity" of the chlorinated pesticides provided the greatest threat to reproductive competence. This application is for the support of two undergraduate and one graduate MBRS students to participate in an ongoing NIH funded research project. The interdisciplinary nature of the research and the multiple techniques involved in its execution provide a unique environment for fostering research interest among undergraduate and graduate students.'